When a person's heart does not function normally due to, for example, a genetic or acquired condition, various treatments may be prescribed to correct or compensate for the condition. For example, pharmaceutical therapy may be prescribed for a patient or a pacemaker or similar device may be implanted in the patient to improve the function of the patient's heart.
In conjunction with such therapy it may be desirable to detect conditions in or apply therapy to one or more chambers of the heart. For example, the health of many patients who have had some form of heart failure (e.g., a heart attack) may deteriorate over time due to progressive failure of the heart. To compensate for the reduction in heart function due to damaged heart tissue, the walls of the heart wall may thicken thereby enabling the heart to pump harder. The resulting enlargement of the heart, however, tends to reduce the ejection fraction of the heart. Progressive heart failure also may affect the timing of contractions in the heart. For example, the normally coordinated pumping of the right ventricle and the left ventricle may become unsynchronized.
The problems caused by progressive heart failure may eventually lead to acute decompensation and associated pulmonary-related conditions. For example, when the function of the left ventricle is compromised (e.g., the left ventricle ejects less blood), the pressure in the left atrium may rise due to a buildup in fluid returning from that portion of the venous system. The rise in left atrial pressure may, in turn, cause fluid to accumulate in the patient's lungs (a condition known as pulmonary edema). Fluid accumulation in the lungs may impair the delivery of oxygen to and the elimination of carbon dioxide from the cardiovascular system and cause hyperventilation or other breathing difficulties, thereby increasing the oxygen demand of the patient. This, in turn, may lead to the patient experiencing shortness of breath or other respiratory problems. If left untreated, such a condition may further exacerbate heart failure.
In view of the above, a rise in left atrial pressure has been proposed as a potential indicator of left ventricular failure. To this end, it had been proposed to implant a pressure sensor in the left atrium. Access to the left atrium may be obtained by initially routing a lead into the right atrium using well known techniques and then routing the lead through the septal wall that separates the right atrium from the left atrium.
In practice, a pressure sensor may need to be calibrated on a regular basis to maintain the accuracy of the corresponding pressure readings. For example, the pressure reading provided by the sensor in response to a given pressure may change over time due to limitations in the design and construction of the sensor (a condition known as sensor drift). To account for this problem, a sensor may be employed in conjunction with a compensation mechanism. For example, the compensation mechanism may automatically calibrate the pressure readings provided by the sensor by comparing the pressure reading with a known pressure such as ambient pressure.
In practice, a typical implanted pressure sensor may not be automatically calibrated in this manner due to the relative difficulty of readily obtaining access to ambient pressure to provide a reference pressure. Consequently, there is a need for improved techniques for detecting left atrial pressure.